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炎症と免疫抑制をプログラムし,RASと協力する

Roderik M Kortlever1, Nicole M Sodir1, Catherine H Wilson2

  • 1Department of Biochemistry, University of Cambridge, 80 Tennis Court Road, Cambridge CB2 1GA, UK; Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA 94143, USA.

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まとめ

KRasとMycの腫瘍遺伝子は 腫瘍の微小環境を再プログラムすることで 癌を誘発します CCL9とIL-23の信号を遮断すると,腫瘍の成長が抑制され,治療目標が明らかになる.

キーワード:
CCL9 についてIL-23 についてマイクNK細胞ラス免疫抑制炎症肺がん腫瘍遺伝子の協力腫瘍の微小環境

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科学分野:

  • 腫瘍学
  • 免疫学
  • 分子生物学

背景:

  • KRasとMycの腫瘍遺伝子は 腫瘍形成に協力しています
  • 腫瘍の進行を促すKras- Mycの協力の正確なメカニズムは完全に理解されていません.
  • 腫瘍の微小環境の役割を理解することは 効果的ながん治療法の開発に不可欠です

研究 の 目的:

  • KRasとMycが腫瘍形成に協力するメカニズムを解明する.
  • 腫瘍の進行中にストロマの再プログラムに関与する重要な信号経路を特定する.
  • KRas駆動肺がんモデルでこれらの経路を標的とした治療の可能性を評価する.

主な方法:

  • KRasG12D駆動性腺腫のマウス肺がんモデルを使用した.
  • Mycの共同活性化が腫瘍の成長,増殖,侵入に及ぼす影響を調査した.
  • 腫瘍ストロマの組成と免疫パターンを分析した.
  • ストロマの再プログラムに責任を負う上皮由来のシグナリング分子 (CCL9とIL-23) を特定し,特徴づけました.
  • 腫瘍進行に対するCCL9とIL-23の共阻害の影響を評価した.
  • Mycの無効化が確立した腫瘍と構造の変化に及ぼす影響を調べました.
  • 腫瘍回帰におけるT細胞とNK細胞の役割を評価した.

主要な成果:

  • KRas誘導のアデノマにおけるMycの共同活性化は,侵襲性アデノカルシノマの発症を迅速に促進する.
  • 腫瘍の進行は炎症性,血管新生性,免疫抑制性ストロマによって特徴付けられます.
  • 皮質由来のCCL9とIL-23は,ストロマの再プログラミングを駆動する重要な信号として特定されています.
  • CCL9はマクロファージの募集,血管新生,PD- L1依存性T細胞とB細胞の排除を媒介する.
  • IL-23は適応性T細胞とB細胞,そしてNK細胞の排除を誘導する.
  • CCL9とIL-23の共阻害はMyc誘発の腫瘍進行を効果的に阻害する.
  • 確立した腫瘍におけるMycの無効化は,構造変化の急速な逆転と腫瘍の回帰につながります.
  • Mycの無効化による腫瘍回帰はCD4+CD8+T細胞とは無関係であるが,NK細胞に依存する.

結論:

  • Mycは腫瘍のストロマを徹底的に再プログラムし 腫瘍の進行に不可欠な免疫抑制環境を作り出します
  • CCL9とIL-23を標的にすることは,KRas主導の肺がんに対する有望な治療戦略です.
  • 腫瘍遺伝子と腫瘍の微小環境の相互作用は 癌の発達と進行において極めて重要です
  • NK細胞は,腫瘍シグナル伝達が停止した後の腫瘍の回帰に重要な役割を果たします.